When cardiac stimulation occurs, the sympathetic nervous system also changes vascular resistance in the periphery. Sympathetic nervous system–mediated vasoconstriction increases vascular resistance and thereby diverts blood away from the skin, kidneys, splanchnic regions, and inactive
Cardiac output (L/min) 22 18 14 10 6 2 0.25 1 2 3 4 O2 uptake (L/min) Skin Heart and brain Viscera Muscle Maximum Vo2 .
•Fig. 19.16 ApproximatedistributionofcardiacoutputatrestandatdifferentlevelsofexerciseuptothemaximalO2consumption(V˜O2)in 0 0 5 10 15 800 1600 0.006 0.010 0.014 60 100 140 180 5 10 15 90 100 110 60 100 140 180 Mean Systolic pressure Diastolic pressure anormalyoungman.(RedrawnfromRuchHP,PattonTC.Physiology and Biophysics. 12thed.Philadelphia:Saunders;1974.)
Fig. 19.16 ). This increase in vascular resistance persists throughout the period of exercise.
Cardiac output and blood flow to active muscles increase as the intensity of exercise increases. Blood flow to the myocardium increases, whereas flow to the brain is unchanged. Blood flow in the skin initially decreases during exercise, then increases as body temperature rises with increments in the duration and intensity of exercise, and finally decreases when the skin vessels constrict as total body O2 consumption nears its maximal value (see
Fig. 19.16
The major circulatory adjustment to prolonged exercise occurs in the vasculature of the active muscles. Local formation of vasoactive metabolites causes marked dilation of the resistance vessels. This dilation progresses with increases in the intensity of exercise. Potassium is one of the vasodilator substances released by the contracting muscle, and this ion may be partly responsible for the initial decrease in vascular resistance in the active muscles. Other contributing factors may be the release of adenosine and a decrease in tissue pH during sustained exercise. The local accumulation of metabolites causes the terminal arterioles to relax, and blood flow through the muscle may increase 15to 20-fold above the resting level. This metabolic vasodilation of the precapillary vessels in active muscles occurs very soon after the onset of exercise. The decrease in TPR enables the heart to pump more blood at a lesser load, and it pumps more efficiently than if TPR were unchanged (see •Fig. 19.17 Effectsofdifferentlevelsofexercise(i.e.,work)onseveralcardiovascularvariables.(DatafromCarlstenA,GrimbyG.The Circulatory Response to Muscular Exercise in Man. Springfield,
IL:CharlesCThomas;1966.)
Marked changes in the capillary circulation also occur during exercise. At rest, only a small percentage of the capillaries are perfused, whereas in actively contracting muscle, all or nearly all of the capillaries contain flowing blood (capillary recruitment). The surface area available for exchange of gases, water, and solutes is increased many times. Furthermore, hydrostatic pressure in the capillaries is increased because of relaxation of the resistance vessels. Hence, water and solutes move into the muscle tissue. Tissue pressure rises and remains elevated during exercise as fluid continues to move out of the capillaries; this tissue fluid is carried away by the lymphatic vessels. Lymph flow is increased as a result of the rise in capillary hydrostatic pressure and the massaging effect of the contracting muscles on the valve-containing lymphatic vessels (see
Contracting muscle avidly extracts O2 from the perfusing blood and thereby increases the arteriovenous O2 difference (